Interstitial tears of the anterior cruciate ligament (ACL) do not heal. We have focused our studies on the fundamental biological explanation for this deficit. Traditional explanations put forward to not seem adequate. Results with our partial laceration model suggest that the biomechanical explanations and synovial "hostile environment" explanations are not sufficient to explain the observed healing deficiency. Rather, we propose on the basis of our original observations that the fibroblast of the ACL is a transitional cell with morphological features similar to the fibrocartilage cell of the meniscus. The ultrastructural studies and immunocytochemical studies with monoclonal antibodies (Mabs) against fibronectin (Fn) show striking differences between the cells of the ACL and the medial collateral ligament (MCL). The ACL lacks the long cytoplasmic processes seen in the MCL and in most other fibrous connective tissue; rather, it rests in a lacuna-like pool of undifferentiated matrix singularly distinctive and partially resembling cartilage cells. WE believe that this morphological appearance may be predictive of the functional response of these cells to injury. Therefore we propose a series of descriptive studies to evaluate the response of the ACL to growth factors known to facilitate the healing response in skin. It is encouraging in this respect that recent studies by Arnoczky show meniscus healing to be facilitated by fibrin clot, which contains a variety of growth factors able to stimulate chemotaxis, mitogenesis and/or protein synthesis.